The Lancet Commission on pollution and health reported that pollution was responsible for 9 million premature deaths in 2015, making it the world's largest environmental risk factor for disease and premature death. We have now updated this estimate using data from the Global Burden of Diseases, Injuriaes, and Risk Factors Study 2019. We find that pollution remains responsible for approximately 9 million deaths per year, corresponding to one in six deaths worldwide. Reductions have occurred in the number of deaths attributable to the types of pollution associated with extreme poverty. However, these reductions in deaths from household air pollution and water pollution are offset by increased deaths attributable to ambient air pollution and toxic chemical pollution (ie, lead). Deaths from these modern pollution risk factors, which are the unintended consequence of industrialisation and urbanisation, have risen by 7% since 2015 and by over 66% since 2000. Despite ongoing efforts by UN agencies, committed groups, committed individuals, and some national governments (mostly in high-income countries), little real progress against pollution can be identified overall, particularly in the low-income and middle-income countries, where pollution is most severe. Urgent attention is needed to control pollution and prevent pollution-related disease, with an emphasis on air pollution and lead poisoning, and a stronger focus on hazardous chemical pollution. Pollution, climate change, and biodiversity loss are closely linked. Successful control of these conjoined threats requires a globally supported, formal science-policy interface to inform intervention, influence research, and guide funding. Pollution has typically been viewed as a local issue to be addressed through subnational and national regulation or, occasionally, using regional policy in higher-income countries. Now, however, it is increasingly clear that pollution is a planetary threat, and that its drivers, its dispersion, and its effects on health transcend local boundaries and demand a global response. Global action on all major modern pollutants is needed. Global efforts can synergise with other global environmental policy programmes, especially as a large-scale, rapid transition away from all fossil fuels to clean, renewable energy is an effective strategy for preventing pollution while also slowing down climate change, and thus achieves a double benefit for planetary health.
Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.
BACKGROUND: Recent studies have reported associations between particulate air pollution and daily mortality rates. Population-based, cross-sectional studies of metropolitan areas in the United States have also found associations between particulate air pollution and annual mortality rates, but these studies have been criticized, in part because they did not directly control for cigarette smoking and other health risks. METHODS: In this prospective cohort study, we estimated the effects of air pollution on mortality, while controlling for individual risk factors. Survival analysis, including Cox proportional-hazards regression modeling, was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities. RESULTS: Mortality rates were most strongly associated with cigarette smoking. After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 (95 percent confidence interval, 1.08 to 1.47). Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together. Mortality was most strongly associated with air pollution with fine particulates, including sulfates. CONCLUSIONS: Although the effects of other, unmeasured risk factors cannot be excluded with certainty, these results suggest that fine-particulate air pollution, or a more complex pollution mixture associated with fine particulate matter, contributes to excess mortality in certain U.S. cities.
BACKGROUND: Exposure to fine-particulate air pollution has been associated with increased morbidity and mortality, suggesting that sustained reductions in pollution exposure should result in improved life expectancy. This study directly evaluated the changes in life expectancy associated with differential changes in fine particulate air pollution that occurred in the United States during the 1980s and 1990s. METHODS: We compiled data on life expectancy, socioeconomic status, and demographic characteristics for 211 county units in the 51 U.S. metropolitan areas with matching data on fine-particulate air pollution for the late 1970s and early 1980s and the late 1990s and early 2000s. Regression models were used to estimate the association between reductions in pollution and changes in life expectancy, with adjustment for changes in socioeconomic and demographic variables and in proxy indicators for the prevalence of cigarette smoking. RESULTS: A decrease of 10 microg per cubic meter in the concentration of fine particulate matter was associated with an estimated increase in mean (+/-SE) life expectancy of 0.61+/-0.20 year (P=0.004). The estimated effect of reduced exposure to pollution on life expectancy was not highly sensitive to adjustment for changes in socioeconomic, demographic, or proxy variables for the prevalence of smoking or to the restriction of observations to relatively large counties. Reductions in air pollution accounted for as much as 15% of the overall increase in life expectancy in the study areas. CONCLUSIONS: A reduction in exposure to ambient fine-particulate air pollution contributed to significant and measurable improvements in life expectancy in the United States.
CONTEXT: Associations have been found between day-to-day particulate air pollution and increased risk of various adverse health outcomes, including cardiopulmonary mortality. However, studies of health effects of long-term particulate air pollution have been less conclusive. OBJECTIVE: To assess the relationship between long-term exposure to fine particulate air pollution and all-cause, lung cancer, and cardiopulmonary mortality. DESIGN, SETTING, AND PARTICIPANTS: Vital status and cause of death data were collected by the American Cancer Society as part of the Cancer Prevention II study, an ongoing prospective mortality study, which enrolled approximately 1.2 million adults in 1982. Participants completed a questionnaire detailing individual risk factor data (age, sex, race, weight, height, smoking history, education, marital status, diet, alcohol consumption, and occupational exposures). The risk factor data for approximately 500 000 adults were linked with air pollution data for metropolitan areas throughout the United States and combined with vital status and cause of death data through December 31, 1998. MAIN OUTCOME MEASURE: All-cause, lung cancer, and cardiopulmonary mortality. RESULTS: Fine particulate and sulfur oxide--related pollution were associated with all-cause, lung cancer, and cardiopulmonary mortality. Each 10-microg/m(3) elevation in fine particulate air pollution was associated with approximately a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively. Measures of coarse particle fraction and total suspended particles were not consistently associated with mortality. CONCLUSION: Long-term exposure to combustion-related fine particulate air pollution is an important environmental risk factor for cardiopulmonary and lung cancer mortality.
Background Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. Methods We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM 2·5 ) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure. Findings Ambient PM 2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM 2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM 2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. Interpretation Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM 2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. Funding Bill & Melinda Gates Foundation and Health Effects Institute.
Plastic pollution accumulating in an area of the environment is considered "poorly reversible" if natural mineralization processes occurring there are slow and engineered remediation solutions are improbable. Should negative outcomes in these areas arise as a consequence of plastic pollution, they will be practically irreversible. Potential impacts from poorly reversible plastic pollution include changes to carbon and nutrient cycles; habitat changes within soils, sediments, and aquatic ecosystems; co-occurring biological impacts on endangered or keystone species; ecotoxicity; and related societal impacts. The rational response to the global threat posed by accumulating and poorly reversible plastic pollution is to rapidly reduce plastic emissions through reductions in consumption of virgin plastic materials, along with internationally coordinated strategies for waste management.
Water quality issues are a major challenge that humanity is facing in the twenty-first century. Here, we review the main groups of aquatic contaminants, their effects on human health, and approaches to mitigate pollution of freshwater resources. Emphasis is placed on chemical pollution, particularly on inorganic and organic micropollutants including toxic metals and metalloids as well as a large variety of synthetic organic chemicals. Some aspects of waterborne diseases and the urgent need for improved sanitation in developing countries are also discussed. The review addresses current scientific advances to cope with the great diversity of pollutants. It is organized along the different temporal and spatial scales of global water pollution. Persistent organic pollutants (POPs) have affected water systems on a global scale for more than five decades; during that time geogenic pollutants, mining operations, and hazardous waste sites have been the most relevant sources of long-term regional and local water pollution. Agricultural chemicals and waste-water sources exert shorter-term effects on regional to local scales.
Environmental exposure to active pharmaceutical ingredients (APIs) can have negative effects on the health of ecosystems and humans. While numerous studies have monitored APIs in rivers, these employ different analytical methods, measure different APIs, and have ignored many of the countries of the world. This makes it difficult to quantify the scale of the problem from a global perspective. Furthermore, comparison of the existing data, generated for different studies/regions/continents, is challenging due to the vast differences between the analytical methodologies employed. Here, we present a global-scale study of API pollution in 258 of the world's rivers, representing the environmental influence of 471.4 million people across 137 geographic regions. Samples were obtained from 1,052 locations in 104 countries (representing all continents and 36 countries not previously studied for API contamination) and analyzed for 61 APIs. Highest cumulative API concentrations were observed in sub-Saharan Africa, south Asia, and South America. The most contaminated sites were in low- to middle-income countries and were associated with areas with poor wastewater and waste management infrastructure and pharmaceutical manufacturing. The most frequently detected APIs were carbamazepine, metformin, and caffeine (a compound also arising from lifestyle use), which were detected at over half of the sites monitored. Concentrations of at least one API at 25.7% of the sampling sites were greater than concentrations considered safe for aquatic organisms, or which are of concern in terms of selection for antimicrobial resistance. Therefore, pharmaceutical pollution poses a global threat to environmental and human health, as well as to delivery of the United Nations Sustainable Development Goals.
Agriculture and urban activities are major sources of phosphorus and nitrogen to aquatic ecosystems. Atmospheric deposition further contributes as a source of N. These nonpoint inputs of nutrients are difficult to measure and regulate because they derive from activities dispersed over wide areas of land and are variable in time due to effects of weather. In aquatic ecosystems, these nutrients cause diverse problems such as toxic algal blooms, loss of oxygen, fish kills, loss of biodiversity (including species important for commerce and recreation), loss of aquatic plant beds and coral reefs, and other problems. Nutrient enrichment seriously degrades aquatic ecosystems and impairs the use of water for drinking, industry, agriculture, recreation, and other purposes. Based on our review of the scientific literature, we are certain that (1) eutrophication is a widespread problem in rivers, lakes, estuaries, and coastal oceans, caused by overenrichment with P and N; (2) nonpoint pollution, a major source of P and N to surface waters of the United States, results primarily from agriculture and urban activity, including industry; (3) inputs of P and N to agriculture in the form of fertilizers exceed outputs in produce in the United States and many other nations; (4) nutrient flows to aquatic ecosystems are directly related to animal stocking densities, and under high livestock densities, manure production exceeds the needs of crops to which the manure is applied; (5) excess fertilization and manure production cause a P surplus to accumulate in soil, some of which is transported to aquatic ecosystems; and (6) excess fertilization and manure production on agricultural lands create surplus N, which is mobile in many soils and often leaches to downstream aquatic ecosystems, and which can also volatilize to the atmosphere, redepositing elsewhere and eventually reaching aquatic ecosystems. If current practices continue, nonpoint pollution of surface waters is virtually certain to increase in the future. Such an outcome is not inevitable, however, because a number of technologies, land use practices, and conservation measures are capable of decreasing the flow of nonpoint P and N into surface waters. From our review of the available scientific information, we are confident that: (1) nonpoint pollution of surface waters with P and N could be reduced by reducing surplus nutrient flows in agricultural systems and processes, reducing agricultural and urban runoff by diverse methods, and reducing N emissions from fossil fuel burning; and (2) eutrophication can be reversed by decreasing input rates of P and N to aquatic ecosystems, but rates of recovery are highly variable among water bodies. Often, the eutrophic state is persistent, and recovery is slow.
BACKGROUND: Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. METHODS AND RESULTS: General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
Environmental pollution studies may be divided into the following broad and somewhat overlapping types.1. Monitoring.Data may be collected (a) to monitor or to characterize ambient concentrations in environmental media (air, water, soil, biota) or (b) to monitor concentrations in air and water effluents.The purpose may be to assess the adequacy of controls on the release or containment of pollutants, Overview of the Design and Analysis Process 3give misleading results when estimating the variance of estimated means, computing confidence limits on means, or deternlining the number of measurements needed to estimate a mean.Other problems that plague environmental data sets are large measurement errors (both random and systematic, discussed in Chapter 2), data near or below measurement detection limits (Chapter 14), missing and/or suspect data values (Chapter 15), complex trends and patterns in mean concentration levels over time and/or space, complicated cause-and-effect relationships, and the frequent need to measure more than one variable at a time.Berthouex, Hunter, and Pallesen (1981) review these types of problems in the context of wastewater treatment plants.They stress the need for graphical methods to display data, for considering the effect of serial correlation on frequency of sampling, and for conducting designed experiments to study cause-and-effect relationships.Schweitzer and Black (1985) discuss several statistical methods that may be useful for pollution data.Many routine monitoring programs generate very large data bases.In this situation it is important to develop efficient computer storage, retrieval, and data analysis and graphical software systems so that the data are fully utilized and interpreted.This point is emphasized by Langford (1978).The development of interactive graphics terminals, minicomputers, and personal computers greatly increases the potential for the investigator to view, plot, and statistically analyze data.In contrast to monitoring programs, some environmental pollution research studies may generate data sets that contain insufficient information to achieve study objectives.Here the challenge is to look carefully at study objectives, the resources available to collect data, and the anticipated variability in the data so that a cost-effective study design can be developed.Whether the study is large or small, it is important to specify the accuracy and precision required of estimated quantities, and the probabilities that can be tolerated of making wrong decisions when using a statistical test.These specifications in conjunction with information on variability can be used to help determine the amount of data needed.These aspects are discussed in Chapters 4-10 and 13. OVERVIEW OF THE DESIGN AND ANALYSIS PROCESSWhen planning an environmental sampling study, one must plan the major tasks required to conduct a successful study.The following steps give an overview of the process.Schweitzer (1982) gives additional discussion relative to monitoring uncontrolled hazardous waste sites.5. Develop a qual ity assurance program pertaining to all aspects of the study, including sample collection, handling, laboratory analysis, data coding and manipulation, statistical analysis, and presenting and reporting results.6. Examine data from prior studies or conduct pilot or base-line studies to approximate the variability, trends, cycles, and correlations likely to be present in the data.7. Develop field sampling designs and sample measurement procedures that will yield representative data from the defined population.S. Determine required statistical data plots, summaries, and statistical analyses, and obtain necessary computer software and personnel for these needs.9. Conduct the study according to a written protocol that will implement the sampling and quality assurance plans.10.Summarize, plot, and statistically analyze the data to extract relevant information and to evaluate hypotheses.11.Assess the uncertainty in estimated quantities such as means, trends, and average maximums.12. Evaluate whether study objectives have been met, and use the newly acquired information to develop more cost-effective studies in the future.1.4
Air Pollutants Effects of Air Pollution Sources of Pollutants in Combustion Processes Gas-Phase Atmospheric Chemistry Aqueous-Phase Atmospheric Chemistry Mass Transfer Aspects of Atmospheric Chemistry Properties of Aerosols Dynamics of Single Aerosol Particles Thermodynamics of Aerosols and Nucleation Theory Dynamics of Aerosol Population Air Pollution Meteorology Micrometeorology Atmospheric Diffusion Theories The Gaussian Plume Equation The Atmospheric Diffusion Equation and Air Quality Models Atmospheric Removal Processes and Residence Times Air Pollution Statistics Acid Rain Index.
Plastic pollution is a pervasive and growing problem. To estimate the effectiveness of interventions to reduce plastic pollution, we modeled stocks and flows of municipal solid waste and four sources of microplastics through the global plastic system for five scenarios between 2016 and 2040. Implementing all feasible interventions reduced plastic pollution by 40% from 2016 rates and 78% relative to "business as usual" in 2040. Even with immediate and concerted action, 710 million metric tons of plastic waste cumulatively entered aquatic and terrestrial ecosystems. To avoid a massive build-up of plastic in the environment, coordinated global action is urgently needed to reduce plastic consumption; increase rates of reuse, waste collection, and recycling; expand safe disposal systems; and accelerate innovation in the plastic value chain.
Efforts to understand and mitigate thehealth effects of particulate matter (PM) air pollutionhave a rich and interesting history. This review focuseson six substantial lines of research that have been pursued since 1997 that have helped elucidate our understanding about the effects of PM on human health. There hasbeen substantial progress in the evaluation of PM health effects at different time-scales of exposure and in the exploration of the shape of the concentration-response function. There has also been emerging evidence of PM-related cardiovascular health effects and growing knowledge regarding interconnected general pathophysiological pathways that link PM exposure with cardiopulmonary morbidiity and mortality. Despite important gaps in scientific knowledge and continued reasons for some skepticism, a comprehensive evaluation of the research findings provides persuasive evidence that exposure to fine particulate air pollution has adverse effects on cardiopulmonaryhealth. Although much of this research has been motivated by environmental public health policy, these results have important scientific, medical, and public health implications that are broader than debates over legally mandated air quality standards.
In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
One of our era's greatest scourges is air pollution, on account not only of its impact on climate change but also its impact on public and individual health due to increasing morbidity and mortality. There are many pollutants that are major factors in disease in humans. Among them, Particulate Matter (PM), particles of variable but very small diameter, penetrate the respiratory system via inhalation, causing respiratory and cardiovascular diseases, reproductive and central nervous system dysfunctions, and cancer. Despite the fact that ozone in the stratosphere plays a protective role against ultraviolet irradiation, it is harmful when in high concentration at ground level, also affecting the respiratory and cardiovascular system. Furthermore, nitrogen oxide, sulfur dioxide, Volatile Organic Compounds (VOCs), dioxins, and polycyclic aromatic hydrocarbons (PAHs) are all considered air pollutants that are harmful to humans. Carbon monoxide can even provoke direct poisoning when breathed in at high levels. Heavy metals such as lead, when absorbed into the human body, can lead to direct poisoning or chronic intoxication, depending on exposure. Diseases occurring from the aforementioned substances include principally respiratory problems such as Chronic Obstructive Pulmonary Disease (COPD), asthma, bronchiolitis, and also lung cancer, cardiovascular events, central nervous system dysfunctions, and cutaneous diseases. Last but not least, climate change resulting from environmental pollution affects the geographical distribution of many infectious diseases, as do natural disasters. The only way to tackle this problem is through public awareness coupled with a multidisciplinary approach by scientific experts; national and international organizations must address the emergence of this threat and propose sustainable solutions.
Plastic particles are ubiquitous pollutants in the living environment and food chain but no study to date has reported on the internal exposure of plastic particles in human blood. This study's goal was to develop a robust and sensitive sampling and analytical method with double shot pyrolysis - gas chromatography/mass spectrometry and apply it to measure plastic particles ≥700 nm in human whole blood from 22 healthy volunteers. Four high production volume polymers applied in plastic were identified and quantified for the first time in blood. Polyethylene terephthalate, polyethylene and polymers of styrene (a sum parameter of polystyrene, expanded polystyrene, acetonitrile butadiene styrene etc.) were the most widely encountered, followed by poly(methyl methacrylate). Polypropylene was analysed but values were under the limits of quantification. In this study of a small set of donors, the mean of the sum quantifiable concentration of plastic particles in blood was 1.6 µg/ml, showing a first measurement of the mass concentration of the polymeric component of plastic in human blood. This pioneering human biomonitoring study demonstrated that plastic particles are bioavailable for uptake into the human bloodstream. An understanding of the exposure of these substances in humans and the associated hazard of such exposure is needed to determine whether or not plastic particle exposure is a public health risk.
Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.
In the 1930s, 40s, and 50s, several episodes of extreme air pollution focused attention on the potential for adverse health effects of air pollution. These included an episode in the Meuse Valley, Belgium, in December 1930 ( 15), an episode in Donora, Pennsylvania in 1948 (36), and several episodes in